The COVID virus can cause the body to attack itself

January 29, 2021 – An international team of researchers studying COVID-19 made a surprising and fundamental discovery: the virus appears to make the body manufacture weapons to attack its own tissues.

The discovery may unravel a number of COVID’s clinical mysteries. They include the intriguing collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after the virus has been eliminated, a phenomenon called long COVID; and why some children and adults have a severe inflammatory syndrome, called MIS-C or MIS-A, after their infections.

“This suggests that the virus may be directly causing autoimmunity, which would be fascinating,” says study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford University in Stanford, CA.

The study also opens up the question of whether other viruses can also break the body’s tolerance of itself, leading people to autoimmune diseases like multiple sclerosis, rheumatoid arthritis and lupus later in life.

Utz says he and his team will study flu patients to see if the virus can also cause this phenomenon.

“My prediction is that it will not be specific only for SARS-CoV-2. I am willing to bet that we will find this with other respiratory viruses, ”he says.

The study comes in the wake of a handful of smaller, more detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania and one in Germany.

The researchers used blood tests to study their immune responses as the infections progressed. The researchers looked for autoantibodies – weapons of the immune system that become violent and launch an attack against the body’s own tissues. They compared these autoantibodies to those found in people who were not infected with the virus that causes COVID.

As previous studies found, autoantibodies were more common after COVID – 50% of people hospitalized because of their infections had autoantibodies, compared to less than 15% of healthy, uninfected people.

Some people with autoantibodies showed little change as the infections progressed. This suggests that autoantibodies were there to begin, possibly allowing the infection to lose control in the body.

“Your body is set up to have bad COVID, and this is probably caused by autoantibodies,” says Utz.

But in others, about 20% of people who had them, autoantibodies became more common as the infection progressed, suggesting that they were directly related to the viral infection, rather than being a pre-existing condition.

Some of them were antibodies that attack key components of the immune system’s weapons against the virus, such as interferon. Interferons are proteins that help infected cells to call for backup and can also interfere with the virus’s ability to copy itself. Eliminating them is a powerful evasive tactic, and previous studies have shown that people who were born with genes that cause them to have less interferon function, or that make autoantibodies against these proteins, appear to be at a higher risk of life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” says study author John Wherry, PhD, who runs the University of Pennsylvania’s Institute of Immunology.

“Now your immune system, instead of having a small hill to climb, is looking at Mount Everest. This is really tortuous. “

In addition to those that neutralize the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders

Utz says he started the study after seeing COVID patients with strange sets of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, muscle pain, brain swelling, dry eyes, blood which clots easily and inflamed blood veins.

“One thing that is very important to note is that we do not know whether these patients will develop autoimmune diseases,” says Utz. “I think we will be able to answer that question in the next 6 to 12 months, as we follow the long haulers and study their samples.”

Utz says it will be important to study autoantibodies on long-haul trucks to see if they can identify exactly which ones appear to be working in the condition. If you can detect them early, it may be possible to treat people at risk for persistent symptoms with drugs that suppress the immune system.

What that means, he says, is that COVID will be with us for a long, long time.

“We need to realize that this virus will cause long-term damage to survivors. Not just long haulers, but everyone who has lung and heart damage and everything. We will study this virus and its evil for decades ”, says Utz.

Sources

BioRxiv, January 29, 2021.

Paul Utz, MD, professor, immunology and rheumatology, Stanford University, Stanford, CA.

John Wherry, PhD, chair of the Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia.


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